Convergence and extension movements are evolutionarily conserved morphogenetic behaviours that elongate tissues in many contexts in animal embryogenesis and organogenesis. Drosophila germ-band extension is a well-studied example that deforms the germ-band epithelium, a thin monolayer of cells tesselating the surface of the ellipsoidal embryo. Extension is driven by the combination of two temporally coordinated mechanisms. A pull from the posterior of the embryo drives extension of the tissue towards the posterior. Meanwhile, a planar polarised distribution of actin and Myosin II motors drives active cell rearrangements within the tissue, driving convergence in the dorso-ventral axis.

Our initial work focused on precise descriptions of cell behavioral dynamics in the germ-band epithelium, for which we developed automated cell tracking and 2D tensorial methods to quantify tissue and cell shape deformation rates, from which a cell rearrangement tensor could be derived1. Tissue deformation is dominated by cell rearrangements and cell shape change, since there is no growth in this tissue and cell divisions don't contribute until late on. Having quantified strains in detail we set about inferring the likely stresses causing our observed strain patterns. Gradients of cell shape stretch and area increase showed that a posterior pull was likely to drive the initial fast phase of extension2, and we have recently shown that this is driven by the posterior mid-gut invagination3.

There were also intriguing periodicities along the anterior-posterior (AP) embryonic axis in the rate of cell intercalation, so in recent work we have been analysing the temporal dynamics of Myosin II polarization, responsible for intrinsic stresses, to understand this pattern formation. We confirm that at the onset of germ-band extension, Myosin II is enriched at AP cell-cell interfaces. As the tissue extends due to cell intercalation, increasing the number of cells in AP, enrichment emerges at boundaries every two to three cells along the AP embryonic axis. Myosin II is localized at boundary interfaces and not the intervening interfaces, irrespective of interface orientation, arguing against the role of global signals. Furthermore, we show that polarized cell rearrangements occur primarily at these boundaries. Myosin II-enriched boundaries therefore provide a single mechanism for simultaneously limiting cell intermingling and driving cell rearrangements during axis extension. Finally, I will speculate on the logic of the combinatorial gene expression code that generates robust periodic Myosin II patterns.